Objective: We evaluated the safety and efficacy of lipoprotein apheresis (LA) in patients with familial hypercholesterolemia (FH) who can't reach low-density lipoprotein cholesterol(LDL-C) target goals with the maximal tolerated dose of lipid-lowering agents. Methods: This was a retrospective cross-sectional study. Between February 2015 and November 2019, patients with FH who were admitted in Fuwai hospital and treated with LA were consecutively enrolled. Based on intensive lipid-lowering agents, these patients received LA by double filtration plasma pheresis (DFPP) method. The changes of lipid levels such as LDL-C and lipoprotein(a)[Lp(a)] were compared before and after LA treatment, and the changes of immunoglobulin (Ig) concentration and LA-related adverse effects were also discussed. Results: A total of 115 patients with FH were enrolled in this study, of which 8 cases were homozygous FH and 107 cases were heterozygous FH. The age was (43.9±12.2) years and there were 75 (65.2%) males, and 108 (93.8%) with coronary artery disease. For pre-and immediately after LA treatment, the LDL-C was (5.20±2.94) mmol/L vs. (1.83±1.08) mmol/L, Lp(a) concentration was 428.70(177.00, 829.50)mg/L vs. 148.90(75.90, 317.00) mg/L (P<0.001), with a decrease of 64.2% and 59.8% respectively. The levels of IgG and IgA measured 1 day after LA treatment were both in the normal range and IgM concentration was below the reference value, the reductions of which were 15.1%, 25.0% and 58.7% respectively (P<0.001). Six patients had mild symptoms of nausea, hypotension dyspnea and palpitation, the symptoms were relieved by symptomatic treatment. Conclusion: For patients with FH who do not achieve LDL-C target goal with the maximal tolerated lipid-lowering agents, especially those with elevated Lp(a) levels, LA, which can significantly further reduce LDL-C and Lp(a) levels, is an effective and safe option.
Adult ; Blood Component Removal/methods* ; Cholesterol, LDL ; Cross-Sectional Studies ; Female ; Humans ; Hyperlipoproteinemia Type II/therapy* ; Lipoprotein(a)/chemistry* ; Lipoproteins/chemistry* ; Male ; Middle Aged ; Retrospective Studies

OBJECTIVETo observe the effects of Yifuning (YEN) capsule on blood lipids of ovariectomized hyperlipidemia rats.

METHODFifty-six female mature Sprague-Dawley rats were randomized into 7 groups: normal control group, model control group, diethylstilbestrol tablets (DT) group, Xuezhikang group, YFN high, middle and low dose groups. The ovariectomized rats were fed on high fat diet and administrated with the drugs for 3 weeks, then were killed and estimated body weight, liver index and five items of blood lipid (TC, TG, HDL-C, LDL-C, VLDL) by test kit. Enzyme (such as HP, LDL, and whole lipase) was detected too.

RESULTThe weight and liver index of model control group increased obviously as compared with normal group. YFN could reduce TG, TC, and LDL-C (P < 0.05) of ovariectomized hyperlipidemia rats obviously and increase HP, LDL and whole lipase (P < 0.05) on the other hand.

CONCLUSIONYFN can ameliorate blood lipids of ovariectomized hyperlipidemia rats.

Animals ; Capsules ; Curcuma ; chemistry ; Drug Combinations ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Female ; Hyperlipidemias ; blood ; Lipase ; blood ; Lipids ; blood ; Lipoprotein Lipase ; blood ; Materia Medica ; isolation & purification ; pharmacology ; Ovariectomy ; Oviducts ; chemistry ; Random Allocation ; Ranidae ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate polymorphisms in the gene for lipoprotein lipase (LPL) in Chinese populations with coronary heart disease (CHD) and to inquire into the relationship between these polymorphisms in LPL gene and CHD.

METHODSGenomic DNA was extracted from patients with CHD and normal control subjects using a salting out method. The entire coding region and flanking sequences of all coding exons of the LPL gene were amplified by PCR technique and PCR products were detected by denaturing high-performance liquid chromatography (DHPLC) and sequenced with a dideoxy terminal termination method.

RESULTSA novel polymorphic site, G830A, that is within the fifth exon of the LPL gene was found. The 192 codon CGA was changed into CAA and resulted in the substitution of glutamine for arginine. Between the control and CHD groups, chi-square test showed no significant difference in the frequencies of the A/A genotype and A allele (P > 0.05). However, the frequencies of A/A genotype and A allele (0.653 and 0.786) in CHD patients with high plasma triglyceride/lowed plasma high density lipoprotein cholesterol were higher than those (0.415 and 0.642) in CHD patients without hyperlipidemia (P < 0.05).

CONCLUSIONNo direct association was found between the LPL Arg192-->Gln substitution polymorphism and CHD, but there is a significant positive correlation between the A/A genotype of the LPL gene and CHD associated with high triglyceride/lowed high density lipoprotein cholesterol. This study may provide new data for exploring the molecular mechanism of CHD.

Alleles ; Apolipoproteins ; blood ; Cholesterol, HDL ; blood ; Chromatography, High Pressure Liquid ; methods ; Coronary Disease ; blood ; enzymology ; genetics ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Gene Frequency ; Humans ; Hypertriglyceridemia ; blood ; genetics ; Lipoprotein Lipase ; genetics ; Lipoproteins ; blood ; Polymorphism, Genetic

OBJECTIVETo determine the genomic structure of low density lipoprotein receptor related protein 5 (LRP5) gene.

METHODScDNA sequence encoding LRP5 was used to screen genomic clones containing LRP5 gene by computer hybridization approach. By comparing the cDNA sequence of LRP5 with the genomic sequences, the genomic structure of LRP5 was determined, and then it was conformed by amplifying and sequencing the sequences of exons and splicing junction.

RESULTSThe genomic sequence of LRP5 gene was 131.6 kb in length, containing 23 exons and 22 introns. Three single nucleotide polymorphisms were detected within the coding sequences of LRP5 gene, namely A459G in exon 2, C2220T in exon 10 and G4416C in exon 21. Four polymorphic markers, D11S1917, D11S4087, D11S1337 and D11S4178, located in the 5' flank sequence, introns 1, 4, and 13 of the LRP5 gene, respectively.

CONCLUSIONThe characterization of genomic structure of LRP5 gene allows the investigators to detect disease-causing mutation within the gene and further study the function of LRP5 gene.

Base Sequence ; DNA ; chemistry ; genetics ; Exons ; Genes ; genetics ; Humans ; Introns ; LDL-Receptor Related Proteins ; Low Density Lipoprotein Receptor-Related Protein-5 ; Polymorphism, Single Nucleotide ; Receptors, LDL ; genetics ; Sequence Analysis, DNA

OBJECTIVETo study on the regulatory mechanism of lipid metabolism disorders in the blood fat of hyperlipemia rat model with Olive Antihyperlipidemia capsule, and do systematic observation on the functions of this medicine on low And high density lipoprotein receptor in rat liver gene expression, and then to clarify the mechanism of action of this medicine on treating hyperlipemia.

METHODTo select SD rat as investigated subject. The hyperlipemia rat models were made with feeding high-fat forage and were randomly divided into six groups based on the total cholesterol level at the ratsfasting for 12 hours: group A, B, C, D, E and group F. The samples in the research were collected and analyzed the changes of LDLR/SR-B1 gene expression in rat's liver by RT-PCR.

RESULTOlive Antihyperlipidemia capsule can markedly enhance LDLR/SR-B1 gene expression in rat's liver and finally accomplish the purpose of reducing blood fat. The experiment shows this medicine has the remarkable effect on hyperlipidemia and proved the theoretical system of treating hyperlipemia for curing the liver is correct.

CONCLUSIONOlive Antihyperlipidemia capsule has an applicable value on preventing the cause, enhance LDLR/SR-B1 gene expression in rat's liver and finally accomplish the purpose of reducing blood fat and development of hyperlipemia and its complications.

Animals ; Capsules ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Gene Expression Regulation ; drug effects ; Hyperlipidemias ; genetics ; pathology ; prevention & control ; Hypolipidemic Agents ; isolation & purification ; pharmacology ; Lipoproteins, HDL ; genetics ; Liver ; metabolism ; Male ; Olea ; chemistry ; Plants, Medicinal ; chemistry ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, LDL ; genetics ; Receptors, Lipoprotein ; genetics ; Scavenger Receptors, Class B ; genetics

3'-Deoxyadenosine, so-called cordycepin, is a bioactive component of the fungus Cordyceps militaris. It has been known to exhibit multiple-biological effects including: modulation of immune response, inhibition of tumor growth, hypotensive and vasorelaxation activities, and promoting secretion of adrenal hormone. To investigate its lipid-lowering effect, hyperlipidemic hamsters and rats fed by high-fat diet were both administered orally with cordycepin extracted from Cordyceps militaris for four weeks. The levels of lipids in hamsters and rats were measured enzymatically before and after the administration of cordycepin (12.5, 25 and 50 mg x kg(-1)). The results suggested that levels of serum total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) increased markedly in the two animal models by feeding high-fat diet. Meanwhile, cordycepin reduced levels of serum TC, TG, LDL-C, VLDL-C as well as LDL-C/HDL-C (high density lipoprotein cholesterol) and TC/HDL-C ratios. In concert with these effects, an increase in lipoprotein lipase (LPL) and hepatic lipase (HL) activity afforded by cordycepin was considered to contribute to the regulation on lipid profiles. Furthermore, no toxicity of cordycepin was observed by intragastric administration at the maximal tolerant dose in ICR mice for 14 days. The exact lipid-lowering effect of cordycepin needs further investigation.
Animals ; Cholesterol ; blood ; Cholesterol, LDL ; blood ; Cholesterol, VLDL ; blood ; Cordyceps ; chemistry ; Cricetinae ; Deoxyadenosines ; adverse effects ; isolation & purification ; pharmacology ; Hyperlipidemias ; blood ; Hypolipidemic Agents ; isolation & purification ; pharmacology ; Lipase ; blood ; Lipids ; blood ; Lipoprotein Lipase ; blood ; Male ; Mesocricetus ; Mice ; Mice, Inbred ICR ; Rats ; Rats, Wistar ; Triglycerides ; blood

OBJECTIVETo investigate the relationship between G1025C (Try316Ser) polymorphism in exon 8 of apolipoprotein H (apoH) gene and stroke and to evaluate the effect of G1025C(Try316Ser) polymorphism on plasma lipid levels in Changsha Hans.

METHODSG1025C (Try316Ser) polymorphism in apoH gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 260 patients with stroke, and 20 stroke pedigrees. Serum antiphospholipid antibody (APA) levels were tested by enzyme linked immunosorbent assay (ELISA). Plasma lipid levels were measured by routine methods.

RESULTSNo statistically significant differences were found in frequencies of genotypes and alleles of G1025C (Try316Ser) polymorphism between the controls and stroke patients. The serum levels of TG in the GC genotype of cerebral infarction patients and controls were markedly higher than those in GG genotype.

CONCLUSIONThere was no association betweenG1025C (Try316Ser) polymorphism and stroke in Changsha Hans. G1025C (Try316Ser) polymorphism was associated with plasma lipid metabolism in Changsha Hans.

Adult ; Aged ; Alleles ; Apolipoprotein A-I ; blood ; Apolipoprotein B-100 ; Apolipoproteins B ; blood ; Base Sequence ; Cerebral Hemorrhage ; complications ; Cerebral Infarction ; complications ; China ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Female ; Gene Frequency ; Genotype ; Glycoproteins ; genetics ; Humans ; Lipids ; blood ; Lipoprotein(a) ; blood ; Male ; Middle Aged ; Mutation, Missense ; Polymorphism, Genetic ; Polymorphism, Single-Stranded Conformational ; Stroke ; blood ; etiology ; genetics ; Triglycerides ; blood ; beta 2-Glycoprotein I